We have found that streptomycin, and erythromycin all block initiating ribosomes at some reaction shortly after initiation. We shall try to determine the blocked reaction for each, and to obtain further evidence for our conclusion that cyclic reinitiation by these unstably blocked ribosomes accounts for the dominance of sensitivity over resistance. We also aim to determine whether the damaging effect of streptomycin on the cell membrane is due to attachment of the altered ribosomes to the membrane; to explore the misreading effect of streptomycin on polysomal but not on initiating ribosomes; and to compare the reversibility of binding of streptomycin to these two kinds of ribosomes. In the ribosome cycle, we plan to try to clarify discrepant results on the presence or absence of a difference in dissociability of ribosomes being released from polysomes or accumulated after that release, and to analyze the possible differences between the initiating native subunits found in lysates and the initiating subunits formed in vitro. Attempts at photoaffinity labeling of binding sites on ribosomes will be continued, and will be extended to streptomycin. Labeling of ligands with a hapten will be attempted, in order to determine whether the labeled region of the ligand is buried or is accessible to antibody. If the latter, we will attempt to identify the region of the ribosome covered by the antibody.